Restenosis after carotid endarterectomy (CEA) limits its long-term efficacy for stroke prevention. Thus, it is of utmost importance to identify the factors that predispose a patient to restenosis after CEA. This systemic review aims to survey the current literature regarding restenosis after CEA and discuss the predictive value of carotid plaque features.
A systemic review of studies on the predictive value of carotid plaque features for restenosis after CEA was conducted according to the PRISMA guidelines. PubMed/MEDLINE and Embase databases were searched up to March 20, 2020. Two authors independently extracted the data and assessed the risk of bias with the Quality in Prognosis Studies tool. Given the heterogeneity in the measurement of prognostic factors, types of CEA, and clinical outcomes, a qualitative synthesis was performed.
Twenty-one articles with a sample size that ranged from 11 to 1203 were included in this systematic review. Based on the presence of calcification in original carotid plaques, two progression patterns of restenosis were hypothesized: patients with calcified plaques may experience a temporary increase in the intima-media thickness (IMT) followed by a decrease in IMT after CEA, whereas patients with noncalcified plaques may experience a gradual increase in IMT after CEA. Accordingly, patients with a high calcium score may have a high restenosis rate within 6 months after CEA and a low restenosis rate thereafter. Thus, the late restenosis rate in patients with uniformly echogenic plaques was lower than that in patients with uniformly echolucent plaques. Pathologically, a lipid-rich, inflammatory carotid plaque is associated with a decreased risk of restenosis within 1 year after CEA, mainly owing to the relatively mild reactive intimal hyperplasia at the surgical site and active inflammation in the remaining media and adventitia. Molecular predictors for restenosis included a Mannose-binding lectin 2 genotype, preoperative C-reactive protein, serum homocysteine, apolipoprotein J, vitamin C, and telomere length of carotid plaques.
This review demonstrated that carotid plaque features, including imaging features, cellular composition, and molecular features, are correlated with the risk of restenosis after CEA. A comprehensive evaluation of plaque characteristics may help to stratify the risk of restenosis after CEA.

BACKGROUND: Native or prosthetic arteriovenous (AV) fistulas are preferred for permanent haemodialysis (HD) access. These are marked with circuit steno-occlusive disease leading to dysfunction or even failure. Late failure rates have been reported as high as 50%. Standard angioplasty balloons are an established percutaneous intervention for HD access stenosis. Reported restenosis rates remain high and practice guidelines recommend a wide 6-month primary patency (PP) of at least 50% for any intervention. Neointimal hyperplasia is one of the main causes for access circuit stenosis. Drug eluting balloon (DeB) angioplasty has been proposed as an alternative intervention to reduce restenosis by local drug delivery and possible inhibition of this process.
OBJECTIVE: To systematically assess the reported efficacy and safety of DeB angioplasty in percutaneous management of prosthetic and autologous HD access stenosis.
METHODS: Protocol for the review was developed following the PRISMA-P 2015 statement. An electronic database (Medline, EMBASE, Clinical Trials.gov and Cochrane CENTRAL) search was conducted to identify articles reporting on the use of DeB intervention in HD AV access. Backward and forward citation search as well as grey literature search was performed. The MOOSE statement and PRISMA 2009 statement were followed for the reporting of results. Data from the included studies comparing DeBs with non-DeBs were pooled using a random effects meta-analysis model and reported separately on randomised and non-randomised studies.
RESULTS: Six studies reported on 254 interventions in 162 participants (mean 27 ± 10 SD). The pooled mean and median duration of follow-up was 12 and 13 months (range 6-24 months). These comprised two randomised control trials (RCTs) and four cohort studies. Participant\'s mean age was 64 ± 5 years and 61% were male. Target lesions (TLs) ranged from under 2 mm to 5.9 mm and 51 were reported as de novo stenosis. Device failure described as wasting of the DeB was reported in two studies (55% and 92.8%). At 6 months TL PP was reported between 70% to 97% for DeBs in the RCTs and cohort studies, and 0% to 26% for non-DeBs. TLs treated with DeBs were associated with a higher primary patency at 6 months as compared to non-DeB balloons (RCTs: odds ratio [OR] 0.25, 95% CI 0.08 to 0.77 and I2 = 19%, cohort studies: OR 0.10, 95% CI 0.03 to 0.31 and an I2 = 20%). No procedure-related major or minor complications were reported.
CONCLUSIONS: Current literature reports DeBs as being safe and may convey some benefit in terms of improved rate of restenosis when used to treat AV access disease. However, this body of evidence is small and clinically heterogeneous. A large multicentre RCT may help to clarify the role of DeBs in the percutaneous treatment of AV HD access stenosis.

Advances in medical devices technology now allow the endovascular treatment of stenotic lesions of the intracranial arteries with the help of the implantation of microstents. The technical development in stent, catheter and guidewire technology now allows the application of these devices in the intracranial arteries, where access issues due to difficult anatomy and length of the access pathway pose far more hurdles to accurately, efficiently and safely navigate these devices as compared with the treatment of lesions of the peripheral arteries or the coronary system. Although the efficacy and safety of these procedures show a continuous improvement with decreased periprocedural complication rates, the development of a significant intraluminal stenotic lesion as a result of neointimal hyperplasia induced within the implants remains a serious delayed complication. In this review, the authors give an overview of the factors affecting the development of neointimal hyperplasia and review the currently available possibilities of the prevention as well as the treatment of the already existing intraimplant stenotic lesions.

Since initially described in 1966, radiocephalic fistula or Brescia-Cimino fistula is one of the most commonly performed fistulas in the world of arteriovenous access. The indications for insertion include, but are not limited to, hemodialysis. Although this is a frequently performed procedure, the primary and secondary patency rates and predictors of failure are not well defined. The review of this topic is difficult because of the diversity in reporting and the absence of consensus between series. Following the current published recommendations by the Society of Vascular Surgery regarding standardization of terminology to facilitate meaningful comparison between the diversity of published data, this review is an attempt to summarize and highlight the relevant information with regard to primary patency, secondary patency, and predictors of failure of radiocephalic fistula using the available English literature.

BACKGROUND: Renal failure is a major cause of morbidity in western Europe, with rising prevalence. Vascular access complications are the leading cause of morbidity among patients on haemodialysis. Considering the health care burden of vascular access failure, there is limited research dedicated to the topic.
METHODS: Randomised control trials of medications aimed at improving vascular access patency were identified using a medline search between January 1950 and January 2011.
RESULTS: Thirteen randomised trials were identified, investigating antiplatelets, anticoagulants and fish oil in preserving vascular access patency. Outcomes are presented and reviewed in conjunction with the underlying pathophysiological mechanisms of failure of vascular access.
CONCLUSIONS: Vascular access failure is a complex process. Most clinical trials so far have involved medications primarily aimed at preventing thrombosis. Other contributing pathways such as neointimal hyperplasia have not been investigated clinically. Improved outcomes may be seen by linking future therapies to these pathways.